The subsequent application of high zinc to primary cortical neurons induced the cytoplasmic accumulation and aggregation of SFPQ, leading to the proposal that dysregulation of zinc availability and/or localization in neurons represents a mechanism for the imbalance in the nucleocytoplasmic distribution of SFPQ observed in the neurodegenerative diseases [10] (Figure 3a). This evidence concerns the gene SFPQ and neurodegenerative disease.